SFRS5 purified MaxPab Mouse Polyclonal Antibody
- Known as:
- SFRS5 enriched MaxPab Mouse Polyclonal Antibody
- Catalog number:
- ENZ-006430-B01P
- Product Quantity:
- 0.05mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- SFRS5 purified MaxPab Mouse Polyclonal Antibody
Related genes to: SFRS5 purified MaxPab Mouse Polyclonal Antibody
- Gene:
- SRSF5 NIH gene
- Name:
- serine and arginine rich splicing factor 5
- Previous symbol:
- SFRS5
- Synonyms:
- SRP40, HRS
- Chromosome:
- 14q24
- Locus Type:
- gene with protein product
- Date approved:
- 1993-09-17
- Date modifiied:
- 2016-06-06
Related products to: SFRS5 purified MaxPab Mouse Polyclonal Antibody
Related articles to: SFRS5 purified MaxPab Mouse Polyclonal Antibody
- BackgroundAlzheimer's disease (AD) is a neurodegenerative disorder primarily characterized by progressive cognitive impairment and neuronal damage. The pathogenesis of AD is complex and involves multiple pathological processes. Currently, effective methods for early diagnosis and treatment are lacking.ObjectiveTo identify key pathogenic genes and investigate their roles in Alzheimer's disease, we analyzed transcriptomic data from dermal fibroblasts of AD patients, aiming to assess their potential as novel biomarkers and therapeutic targets.MethodsTranscriptomic data from AD patient and control-derived dermal fibroblasts (DFs) were analyzed to identify differentially expressed genes. Key genes were screened using bioinformatics and a random forest algorithm. ceRNA analysis was performed to explore miRNA-mRNA interactions. The candidate gene SRSF5 was validated via overexpression and knockdown, followed by qPCR, western blotting, and reactive oxygen species (ROS) assays. The role of SRSF5 in endoplasmic reticulum (ER) stress was evaluated by measuring ER stress markers and cellular stress responses.ResultsTranscriptomic analysis revealed significant upregulation of SRSF5 in AD DFs. ceRNA analysis identified miRNAs regulating SRSF5 in AD. Overexpression of SRSF5 led to reduced neuronal proliferation, increased apoptosis, elevated ROS levels, and activation of ER stress markers (CHOP, GRP78, XBP1). SRSF5 knockdown alleviated these effects.ConclusionsSRSF5 may drive AD pathogenesis via ER and oxidative stress, serving as a potential biomarker and therapeutic target for early diagnosis and intervention. - Source: PubMed
Publication date: 2026/04/23
Xie MinNiu XiaoliSun FengleiShi Lin - This study investigates mRNA degradation in human dental pulp to explore its utility for estimating the late postmortem interval (LPMI). Morphological changes in pulp tissue at 0, 7, 14, 21 and 28 days postmortem were observed via HE staining, showing progressive cellular degradation. High-throughput sequencing of samples at 0, 7, and 21 days identified candidate mRNAs. Five mRNA biomarkers were obtained, namely SRSF5, FGFR1, ACADVL, FOS, and LRP1. Their expression levels at 0, 3, 7, 10, 14, 21 and 28 days were quantified using RT–qPCR with 18 S rRNA as the reference gene. Results demonstrated a consistent decrease in all five mRNAs over time. Mathematical models correlating mRNA levels with LPMI were established. Multi-index models exhibited superior fitting accuracy and predictive performance compared to single-index models, as validated using samples from 10, 18 and 25 days postmortem intervals, indicating greater practical applicability. This approach provides a new direction for forensic LPMI estimation research and contributes to the development of forensic pathology. - Source: PubMed
Publication date: 2026/04/13
Yin MuxuanGao HaiboChen JuncaiZou LongqiWang XinruLu ShuhanLi HuanHe FanTang QunWu Hua - The HIV-1 genome [genomic RNA (gRNA)] has an unusually biased nucleotide content and is rich in adenosines. Selective packaging of the gRNA is thought to be driven by specific binding of the nucleocapsid (NC) domain of the viral Gag protein to the packaging signal (Ψ) in the host cell cytosol. However, deletion of regions within Ψ reduces-but does not completely abolish-genome packaging. To probe whether another feature of the gRNA may contribute to the selective gRNA packaging process, we replaced NC with heterologous RNA-binding domains (RBDs) with distinct RNA-binding properties. Surprisingly, despite disparate RNA binding specificities, all Gag-RBD chimeras successfully recruited the gRNA to the plasma membrane, suggesting that the initial gRNA recognition in the cytosol is not rate limiting. Notwithstanding, many chimeras exhibiting G/C binding specificity were arrested at the assembly stage. Only the Gag-SRSF5 chimera, which multimerized efficiently on adenosine-rich sequences on the gRNA, assembled efficiently and packaged gRNA at near wild-type levels. Importantly, rationally designed mutations that altered the A/G-rich binding specificity of Gag-SRSF5 decreased genome encapsidation efficiency. Furthermore, many Gag chimeras displayed potent dominant negative activities, highlighting NC functions as a targetable step in virus replication. Together, our findings reveal an unexpected aspect of the HIV-1 gRNA, its biased nucleotide content, as a key driver of selective genome packaging. - Source: PubMed
Publication date: 2026/04/02
Vuong Hung RZhou QianziL Lesko SydneyTenneti KasyapDavis KeanuScott ShanyquaGuo MomingBoodwa-Ko DaphneEschbach Jenna EGopal KamyaPorter Jessica MWang QiboXia MingBoateng AnthonyWang YiqingMohammed ShawnLee NakyungTelesnitsky AliceM Sherer NathanKutluay Sebla B - tRNA-derived small RNAs (tsRNAs) or tRNA-derived fragments (tRFs) are an important class of regulatory molecules whose role in cardiac hypertrophy remains largely unknown. Here, we identified a novel tRF contributing to the regulation of cardiac hypertrophy that we termed CHAtRF (cardiac hypertrophy-associated tRF). The CHAtRF level was increased in mice and in patients with cardiac hypertrophy. CHAtRF deficiency attenuated angiotensin II (AngII)-induced cardiac hypertrophy and restored the heart function, while CHAtRF overexpression enhanced hypertrophic responses. Mechanistically, CHAtRF directly interacts with SRSF5 and blocks SRSF5 to bind with Psmg4 pre-mRNA, which mediates alternative splicing of Psmg4 pre-mRNA and promotes exon 2 skipping of Psmg4. CHAtRF-dependent alternative splicing of Psmg4 inhibits the expression of Psmg4 full-length isoform, resulting in progression of pathological hypertrophy. The ability of CHAtRF to regulate hypertrophy was confirmed in hiPSC-CMs, and CHAtRF serum levels are higher in individuals with myocardial hypertrophy or heart failure. Our findings reveal new insights into the previously unrecognized role of tsRNAs during cardiac hypertrophy, which provide potential novel therapeutic targets for pathological hypertrophy and might serve as potential biomarkers for diagnosing cardiac hypertrophy and heart failure. - Source: PubMed
Publication date: 2026/03/26
Zhou Lu-YuWang KaiLi Ying-HuiWang Shao-CongChen Xin-ZheLiu Cui-YunLi Xin-MinWang Yu-QinCai Shu-FangYang Su-MinWang Yun-HongLiu FangWang Kun - The pathogenesis of systemic lupus erythematosus (SLE) is closely associated with abnormal activation of B lymphocytes. Telitacicept simultaneously blocks B-cell stimulating factors and proliferation-inducing ligands, thereby inhibiting B-cell proliferation and differentiation, demonstrating favorable therapeutic efficacy in the majority of SLE patients. However, there is a lack of reliable biomarkers of efficacy and systematic elucidation of its mechanism of action. - Source: PubMed
Publication date: 2026/03/04
Nie HuiyuChang SiyuanChen HanhanShi JiahuiLi ShuPeng XiaofeiCheng WeiWang JiaTang QiGe YanXie XiLi Fen